中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2013年
10期
1022-1026
,共5页
陈子民%王涛%姜俊海%沈定荣%高奎乐%王伟
陳子民%王濤%薑俊海%瀋定榮%高奎樂%王偉
진자민%왕도%강준해%침정영%고규악%왕위
冷血心脏停搏液%自体血%未成熟心肌%超氧化物歧化酶%基质金属蛋白酶2
冷血心髒停搏液%自體血%未成熟心肌%超氧化物歧化酶%基質金屬蛋白酶2
랭혈심장정박액%자체혈%미성숙심기%초양화물기화매%기질금속단백매2
Cold%blood%cardioplegia%Autologous%blood%Immature%myocardium%Superoxide%dismutase%Matrix%metalloproteinase-2
目的 对比研究冷自体血心脏停搏液与HTK液(康斯特停搏液)在婴幼儿体外循环室间隔缺损修补术冠状静脉窦回流血中超氧化物歧化酶(SOD)、基质金属蛋白酶2(MMP-2)的浓度变化,揭示其对未成熟心肌的保护作用.方法 ≤1岁行室间隔缺损修补术患儿60例,随机分为A组与B组,各30例.A组于体外循环前经主动脉根部抽取血液配制K+浓度为20 mmol/L的4℃自体血心脏停搏液.A组应用冷自体血心脏停搏液、B组应用HTK液.分别于主动脉阻断前即刻、主动脉开放后第1分钟及第15分钟抽取冠状静脉窦回流血,ELISA法检测SOD、MMP-2浓度,进行统计学处理.结果 SOD、MMP-2两个指标在组内、组间及交互差异均有统计学意义(P均＜0.05),A组和B组两个指标均在主动脉开放后升高.主动脉阻断前,A组和B组间SOD和MMP-2浓度差异均无统计学意义[两组分别为:SOD∶(85.37±16.82) mU/L与(91.51±15.02) mU/L,P ＞0.05; MMP-2∶(362.29±29.52) μg/L与(372.32±31.42) μg/L,P＞0.05]；主动脉开放后1 min,A组和B组间的SOD和MMP-2浓度差异均有统计学意义[两组分别为:SOD:(106.97±17.46) mU/L与(98.74±12.54) mU/L,(P＜0.05)；MMP-2:(439.48±51.62) μg/L与(465.49±48.83) μg/L,P＜0.05]；主动脉开放后15 min,A组和B组间的SOD和MMP-2浓度差异均有统计学意义[两组分别为:SOD:(104.03±12.63) mU/L与(97.94±10.87)mU/L,P＜0.05；MMP-2:(390.16±45.63) μg/L与(425.21±48.24) μg/L,P＜0.05].A组较B组心率失常发生率低(x2=8.223,P＜0.05),正性肌力药物倚赖程度低(x2=4.022,P＜0.05).结论 冷自体血心脏停搏液可促进未成熟心肌SOD的释放、减少MMP-2的产生,更具有保护作用.
目的 對比研究冷自體血心髒停搏液與HTK液(康斯特停搏液)在嬰幼兒體外循環室間隔缺損脩補術冠狀靜脈竇迴流血中超氧化物歧化酶(SOD)、基質金屬蛋白酶2(MMP-2)的濃度變化,揭示其對未成熟心肌的保護作用.方法 ≤1歲行室間隔缺損脩補術患兒60例,隨機分為A組與B組,各30例.A組于體外循環前經主動脈根部抽取血液配製K+濃度為20 mmol/L的4℃自體血心髒停搏液.A組應用冷自體血心髒停搏液、B組應用HTK液.分彆于主動脈阻斷前即刻、主動脈開放後第1分鐘及第15分鐘抽取冠狀靜脈竇迴流血,ELISA法檢測SOD、MMP-2濃度,進行統計學處理.結果 SOD、MMP-2兩箇指標在組內、組間及交互差異均有統計學意義(P均＜0.05),A組和B組兩箇指標均在主動脈開放後升高.主動脈阻斷前,A組和B組間SOD和MMP-2濃度差異均無統計學意義[兩組分彆為:SOD∶(85.37±16.82) mU/L與(91.51±15.02) mU/L,P ＞0.05; MMP-2∶(362.29±29.52) μg/L與(372.32±31.42) μg/L,P＞0.05]；主動脈開放後1 min,A組和B組間的SOD和MMP-2濃度差異均有統計學意義[兩組分彆為:SOD:(106.97±17.46) mU/L與(98.74±12.54) mU/L,(P＜0.05)；MMP-2:(439.48±51.62) μg/L與(465.49±48.83) μg/L,P＜0.05]；主動脈開放後15 min,A組和B組間的SOD和MMP-2濃度差異均有統計學意義[兩組分彆為:SOD:(104.03±12.63) mU/L與(97.94±10.87)mU/L,P＜0.05；MMP-2:(390.16±45.63) μg/L與(425.21±48.24) μg/L,P＜0.05].A組較B組心率失常髮生率低(x2=8.223,P＜0.05),正性肌力藥物倚賴程度低(x2=4.022,P＜0.05).結論 冷自體血心髒停搏液可促進未成熟心肌SOD的釋放、減少MMP-2的產生,更具有保護作用.
목적 대비연구랭자체혈심장정박액여HTK액(강사특정박액)재영유인체외순배실간격결손수보술관상정맥두회류혈중초양화물기화매(SOD)、기질금속단백매2(MMP-2)적농도변화,게시기대미성숙심기적보호작용.방법 ≤1세행실간격결손수보술환인60례,수궤분위A조여B조,각30례.A조우체외순배전경주동맥근부추취혈액배제K+농도위20 mmol/L적4℃자체혈심장정박액.A조응용랭자체혈심장정박액、B조응용HTK액.분별우주동맥조단전즉각、주동맥개방후제1분종급제15분종추취관상정맥두회류혈,ELISA법검측SOD、MMP-2농도,진행통계학처리.결과 SOD、MMP-2량개지표재조내、조간급교호차이균유통계학의의(P균＜0.05),A조화B조량개지표균재주동맥개방후승고.주동맥조단전,A조화B조간SOD화MMP-2농도차이균무통계학의의[량조분별위:SOD∶(85.37±16.82) mU/L여(91.51±15.02) mU/L,P ＞0.05; MMP-2∶(362.29±29.52) μg/L여(372.32±31.42) μg/L,P＞0.05]；주동맥개방후1 min,A조화B조간적SOD화MMP-2농도차이균유통계학의의[량조분별위:SOD:(106.97±17.46) mU/L여(98.74±12.54) mU/L,(P＜0.05)；MMP-2:(439.48±51.62) μg/L여(465.49±48.83) μg/L,P＜0.05]；주동맥개방후15 min,A조화B조간적SOD화MMP-2농도차이균유통계학의의[량조분별위:SOD:(104.03±12.63) mU/L여(97.94±10.87)mU/L,P＜0.05；MMP-2:(390.16±45.63) μg/L여(425.21±48.24) μg/L,P＜0.05].A조교B조심솔실상발생솔저(x2=8.223,P＜0.05),정성기력약물의뢰정도저(x2=4.022,P＜0.05).결론 랭자체혈심장정박액가촉진미성숙심기SOD적석방、감소MMP-2적산생,경구유보호작용.
Objective To investigate the effect of cold autologous blood cardioplegia and HTK solution on changes of superoxide dismutase (SOD) and Matrix metalloproteinase-2 (MMP-2) in infant coronary sinus vein blood,which underwent ventricular septal defect suture in extracorporeal circulation,in order to reveal their protective effect of autologous cold blood cardioplegia on immature myocardium.Methods Sixty cases with ventricular septal defect,aged less 1-year-old,were randomly divided into experimental group (n =30) and control group(n =30).Autologous cold blood cardioplegia was obtained on aortic blood before aortic root draw in extracorporeal circulation with K + concentration of 20 mmol/L and 4 ℃ temperature.The experimental group was used cold autologous blood cardioplegia as arresting and protecting cardioplegia,while the control group used HTK solution.Blood sample from coronary sinus and vein was obtained at immediately before aortic cross-clamping,1 minute and 15 minutes after aortic cross-opening.SOD and MMP-2 levels were determined by enzyme-Linked Immuno Sorbent Assay (ELISA).Results The levels of SOD and MMP-2 levels within the group,between the groups and interaction were significant difference (P ＜ 0.05).After aortic cross-opening,the level of SOD and MMP-2 of the experimental group and the control group were increased (P ＜ 0.05).Before aortic cross-clamping,The activity of SOD in experiment was(85.37 ± 16.82) mU/L,as same as that in the control group((91.51 ± 15.02) mU/L,P ＞ 0.05).The MMP-2 concentration was in experiment group was (362.29 ±29.52) μg/L,as same as that in the control group((372.32 ± 31.42) μg/L,P ＞ 0.05).At 1 minute after aortic cross-opening,there were significant differences regarding of SOD and MMP-2 levels between the both groups(SOD ∶ (106.97 ± 17.46) mU/L vs.(98.74 12.54) mU/L,P ＜ 0.05 ; MMP-2 ∶ (439.48 ± 51.62) μg/L vs.(465.49 ±48.83) μg/L,P ＜0.05) ;The same trend was seen at 15 minutes after aortic cross-opening in two groups in terms of SOD and MMP-2 level (SOD:(104.03 ± 12.63) mU/L vs.(97.94 10.87) mU/L,P ＜0.05; MMP-2:(390.16 ±45.63) μg/L vs.(425.21 ±48.24) μg/L,P ＜0.05).Compare to group B,arrhythmia incidence(x2 =8.223,P ＜ 0.05) and positive inotropic drug dependent degree was lower in group A (x2 =4.022,P ＜ 0.05).Conclusion The cold autologous blood cardioplegia could promote the release of SOD in immature myocardium and reduce the production of MMP-2,which has endogenous protective effect for the infant Imature myocardium.
